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B Ribalet

Publications and source records attributed to B Ribalet.

27 records · Page 2Linked to original sources
PubMed1979

Mouse pancreatic beta-cells: tetraethylammonium blockage of the potassium permeability increase induced by depolarization.

1. Membrane potentials and input resistance were measured in beta-cells from mouse pancreatic islets of Langerhans in the presence or absence of D-glucose. 2. Tetraethylammonium (TEA) (a specific blocker of the K permeability increase induced by shifts in membrane potential from negative to positive values) was externally applied and its effects on potentials and input resistance evaluated. 3. In the absence of glucose, addition of TEA up to 20 mM to the perifusion medium did not affect the resting potential and the input resistance, the selectivity ratio PK/PNa (calculated from the constant field equation) remaining unchanged at about 30. 4. The characteristic response of the beta-cell membrane potential, in the presence of glucose, is a fluctuation between a silent phase at about -50 mV and an active phase at about -40 mV giving rise to a train of spikes. TEA abolishes this pattern and very much reduces the graded response of spike frequency normally seen with different concentrations of glucose. 5. Addition of glucose in the presence of up to 20 mM-TEA induces an increase in membrane resistance of about 4.10(7) omega. 6. TEA lowers the glucose level required to trigger the electrical activity from about 5.6 to about 4.6 mM. 7. TEA blocks the repolarization phase of action potentials induced by the addition of glucose or by depolarizing intracellular current injection. 8. In the presence of 11.1 mM-glucose and 20 mM-TEA the action potentials frequently crossed the zero line, the membrane potential reaching up to 25 mV during the peak of the spikes.

Action Potentials↗
PubMed1979

Potassium permeability activated by intracellular calcium ion concentration in the pancreatic beta-cell.

1. Membrane potentials and input resistance were measured in beta-cells from mouse pancreatic islets of Langerhans in a study designed to assess the role of a K permeability specifically blocked by quinine or quinidine and activated by intracellular calcium ion concentration ([Ca2+])i-activated PK). 2. Addition of 100 microM-quinine to the perifusion medium resulted in a 10--30 mV depolarization of the membrane and an increase in the input resistance of ca. 4.10(7) omega. 3. In the absence of glucose, 100 microM-quinine induced electrical activity. 4. In the presence of glucose, 100 microM-quinine abolished the burst pattern of electrical activity and very much reduced the graded response of spike frequency normally seen with different concentrations of glucose. 5. Addition of mitochondrial inhibitors, KCN, NaN3, DNP, CCCP, FCCP, to the perifusion medium containing glucose rapidly hyperpolarized the beta-cell membrane, inducing a concomitant decrease in input resistance. 6. In the presence of glucose, these mitochondrial inhibitors reversibly blocked electrical activity; upon removal of the inhibitor, recovery of electrical activity followed a biphasic pattern. 7. The effects of mitochondrial inhibitors were partially reversed by 100 microM-quinine. 8. It is proposed that the membrane potential of the beta-cell in the absence of glucose is predominantly controlled by the [Ca2+]i-activated PK. It is further suggested that this permeability to K controls the level for glucose stimulation and leads to the generation of the burst pattern.

Action Potentials↗
PubMed1978

Cyclic changes in potential and resistance of the beta-cell membrane induced by glucose in islets of Langerhans from mouse.

1. The effects of KCl on the membrane potential were studied in cells from mouse islets of Langerhans identified as beta-cells by the characteristic pattern of electrical activity induced by 11.1 mM glucose. 2. In the absence of glucose, when the beta-cell membrane does not exhibit electrical activity, the dependence of the membrane potential upon external potassium [K+]o, could be described by the constant field equation using a PK/PNa ratio between 30 and 75. 3. In 11.1 mM glucose, when the beta-cell membrane potential fluctuates between a silent phase at about -50 mV and an active phase at about -40 mV giving rise to a train of spikes, the dependence of the membrane potential upon [K+]o could also be described with the constant field equation using a smaller PK/PNa of about 15, during the silent phase, and of about 8, during the active phase (foot of the spikes during the burst). 4. A bridge amplifier for measuring the changes in membrane potential during the application of pulses of current through the same micro-electrode was used to estimate the input resistance of a beta-cell. In 11.1 mM glucose, rough estimates of the membrane resistance during the silent phase averaged 1.2 X 10(8) omega. 5. The time course of the changes in input resistance of the cell when switching from 0 to 11.1 mM glucose showed a transient decrease from 0.9 X 10(8) to 0.7 X 10(8) omega followed by an increase to 1.2 X 10(8) omega. 6. The burst pattern was shown to result from the superposition of two potential changes: (a) 5--10 mV depolarization (lasting about 10 sec in 11.1 mM glucose), and (b) 10--50 mM spikes (lasting about 0.1 sec). Only the latter could be suppressed by hyperpolarizing current injection. 7. Application of pulses of current during the various phases of the electrical activity in 11.1 mM glucose enable us to compare the resistance during the silent and active phases. This was found to be oscillating between a high resistance value at about 1.2 X 10(8) omega before each burst and a low resistance value at 0.9 X 10(8) omega during the active phase at the foot of the spikes. In some cells the resistance during the silent phase remained fairly constant. In other cells it increased gradually from 1.1 X 10(8) to 1.3 X 10(8) omega measured just before each burst of spikes. 8. The observed increase in resistance induced by glucose together with the measured dependency of the membrane potential on [K+]o with and without glucose can be explained by postulating that in the presence of glucose the K+ permeability of the beta-cell membrane is reduced. 9. The oscillations between a high and a low resistance state in the presence of 11.1 mM glucose could be due to a sudden decrease in K+ permeability followed by a much larger increase in permeability to other ions, presumably Na+ and Ca2+.

Action Potentials↗